The Role of Hepatitis C Virus Genotypes in Development of Autoimmune Diseases Free

In the study by Betterle et al. (1), it was stated that there was no association between the occurence of organ-specific/nonorgan-specific autoimmune diseases and chronic hepatitis C virus (HCV) infection. It was evident in previous studies (2,3) that there was a clear association among the antigenic subtypes of the HCV, prognosis of disease, autoimmune disease development, and response to the interferon-α (IFN-α) treatment. Also, these studies stress that some specific subtypes, e.g., HCV-1b, may have worse prognosis and poor response to the treatment (4). This result may be due to the fact that the various genotypes of the HCV have various immunological responses in the host. So, it seems logical that the development of the HCV subtype–specific immune response may stimulate the formation of antibodies directed to some organs or may be generalized, which are named organ- and/or nonorgan-specific autoimmune diseases. Therefore, various types of viral antigens may play an important role during the development of the various types of autoimmune diseases via hosts’ immune responses. In the study (1), there were some autoantibody positivity results before IFN-α treatment (one patient with low-titer classic islet cell antibody pattern, one with high levels of anti-GAD antibodies, two with anti–glucagon cell antibody, four with microsomal antibodies, two with thyroglobulin autoantibodies, five with parietal cell antibodies, and—from nonorgan-specific antibody group—two patients with anti-nuclear antibody [ANA] positivity); but, it is not clear which HCV subtypes were infecting antibody-positive patients. Like this situation, the HCV subtype–specific host-immune response may be responsible, as with the autoimmune diseases that developed during IFN-α treatment. Therefore, it would have been useful in this study to assess whether a clinical linkage was present between the viral subtype and autoimmunity.